An upper body fat distribution increases the risk for the metabolic complications of obesity, however, the determinants of regional fat distribution are unknown. Regional differences in adipose tissue fatty acid uptake and/or release must ultimately determine regional fat mass, but the ability to differentially add new adipocytes must also help determine regional fat mass. Adipocyte size can only increase to limited degree beyond which the addition of more fat cells must take place for regional or total fatness to expand. This is a competing supplement to our currently funded grant, the long-term goal of which is to help understand the causes and consequences of differences in body fat distribution. We propose to collect novel information regarding adipose tissue biology in the context of the overfeeding study that will be done as part of the current grant. We have developed new methods to study preadipocyte number and dynamic characteristics. Together with Dr. James Kirkland we propose to assess whether differences in preadipocyte number or function relate to regional fat gain. Per the original proposal, we will test the hypothesis that regional differences in body fat gain in response to overfeeding are associated with regional differences in meal fatty acid uptake. We will determine whether the insulin resistant, non-overweight adults gain more visceral fat during a fixed (2.0 kg) fat gain induced by overfeeding and whether meal fatty acid disposal during overfeeding determines regional fat gain. The new hypothesis we propose to test is that regional differences in the number and/or dynamic characteristics of adipocyte precursors predict regional differences in fat gain. Successful completion of these studies will help us understand the potential role of preadipocytes in the regulation of regional fat distribution. [unreadable] [unreadable]